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What do hallucinogens, starvation and magnets all have in common? No, they’re not the key ingredients for a wild and crazy weekend; they are all potential alternative treatments for depression that are being explored by researchers and clinicians alike.

Scientists have long known that the serotonin theory of depression is imperfect, yet few treatment options are available beyond the standard course of cognitive-behavioral therapy and selective serotonin reuptake inhibitors (SSRIs). In my new piece for Pacific Standard, I explore recent research that has emerged looking at some potential alternatives for depression that are rather… unconventional.

This includes giving people psilocybin, the active ingredient in so-called “magic” mushrooms, which also boosts serotonin levels and crucially taps into the amygdala, the brain’s major emotional center. Another possible avenue involves boosting ghrelin levels in the brain, a hunger hormone that may also play a role in protecting neurons from the destructive effects of stress, particularly in the hippocampus. Alternatively, using high-powered magnets, researchers and clinicians are able to activate certain key parts of the brain that can potentially lead to a suppression of other over-active emotional regions, turning down our feelings of anxiety or depression.

While none of these options is perfect, they do provide an encouraging new perspective, thinking outside the box to treat this condition that will afflict at least one in ten of us at some point in our lives.

You’re running down a hallway; running away from someone? Running towards something? Your feet start to lift off the ground and the ceiling opens up. You float higher and higher, and you get the feeling you’re not alone. You turn to your left and it’s Bob Dylan, laughing and calling you “Mr. Tambourine Man”. Suddenly the balloon you were holding onto, carrying you up into the sky, turns into a tangerine and you start to plummet back to earth. Just before you slam into the ground you awaken; sweaty, sheets twisted, wondering what the hell that was all about.

Dreams are weird. Especially if you’ve eaten a lot of cheese the night before.

Or so says the common myth. From Charles Dickens to Arab Strap, cheese dreams have been a part of our popular culture for over the last 150 years. But is there actually any truth in this old wives’ tale?

A study conducted in 2005 by the British Cheese Board attempted to debunk this claim by giving 200 participants 20 grams (roughly 0.7 ounces) of cheese 30 minutes before they went to bed and asking them to record their dreams and quality of sleep. In the study, 67% of participants recalled their dreams, and none reported the presence of any nightmares, something the Cheese Board is calling a win.

Instead of night terrors, the researchers report that the cheese resulted in pleasant nighttime fantasies in most individuals. They even went so far as to test the varying effects different types of fromage had on an individual’s dream-state. From their conclusions, blue Stilton resulted in the most bizarre trips, affecting about 80% of participants and resulting in visions of talking animals, vegetarian crocodiles and warrior kittens. On the other end of the spectrum, Cheshire cheese produced the least memorable nights, with less than half of the participants being able to recall their dreams.

The study (again, initiated by the cheese industry) also claimed that eating cheese before bed actually helped people fall asleep. This is supposedly due to the relatively high tryptophan content in cheese, an amino acid involved in the production of melatonin (and serotonin), which plays an important role in our sleep-wake cycle.

However, it should be noted that there was no report of a control or placebo group in this experiment, such as participants who ate nothing or consumed a soy cheese sample (yum!) before bed. Thus, there’s no empirical evidence that it was actually the cheese causing these effects and that it was not just the natural sleep state for these individuals.

As for the dream link, there is only one academic paper that mentions the cheese-dream phenomenon, and that is only anecdotally. However, one Internet theory I found (I know, I’m reaching here) proposed that the bacteria and fungal content in cheese, and in potent blue cheeses in particular, might be at the root of the increase in dream vividness. This is due to the potential psychoactive effects different compounds found in fungi, like tryptamine or tyramine, might have, influencing our brains’ chemical systems and thus our state of mind.

Tryptamine is a common chemical precursor for serotonin and other related alkaloids, some of which are involved in the hallucinogenic effects of psilocybin (“magic” mushrooms) and DMT. However, there’s no hard evidence that tryptamine is actually present in the Stiltons and Gorgonzolas of the world, and even if it was, it would be in extremely low doses. After all, when was the last time you felt high after eating cheese?

Conversely, tyramine is a monoamine that works by releasing other neurotransmitters like adrenaline, noradrenaline and dopamine into the body. Another theory is that tyramine’s effect on noradrenaline release in an area of the brain called the locus coereleus, a region important in our sleep-wake cycle, is altering our dream patterns.

Some antidepressants work by inhibiting the breakdown of monoamines (monoamine oxidase inhibitors – MAOIs), and it can be potentially dangerous to eat foods high in tyramine when on this medication as it can result in an excess of these chemicals in your brain and body. The medication mentioned in the old academic paper, pargyline hydrochloride, actually works as an MAOI, potentially explaining the bizarre effect eating cheese had on the patient. There are also reports of foods high in tyramine causing migraines in some individuals, particularly those on MAOIs; however, another study found no evidence of this link.

Finally, there are numerous other types of foods that contain chemical compounds like tyramine and tryptophan affecting our neurotransmitter systems. This includes cured meats, egg whites and soybeans, none of which have the dream-producing reputation of cheese. So for now, it appears to be an untenable link between cheese specifically and these nighttime apparitions.

Then again, I did eat some cheddar last night, which might just explain Bob Dylan’s appearance in my nocturnal activities. According to the Cheese Board, cheddar was linked to visions of celebrities dancing in your head.

My favorite holiday is on Thursday. And while I can’t be at home in the States to celebrate, being an ex-pat at Thanksgiving does have its perks, as I get to attend multiple alternate feasts over the weekend. That means twice the stuffing, twice the cranberries, twice the turkey, twice the tryptophan.

Yes, tryptophan. That infamous amino acid we use to justify dozing off during our aunt’s vacation slideshow after the big meal. Tryptophan is an essential amino acid, a protein precursor that the body uses to build various chemical structures. This includes serotonin, one of the primary neurotransmitters in the brain that is involved in everything from decision-making to depression. Serotonin is also a precursor to melatonin, which is important in sleep and wakefulness and is where the tryptophan-tiredness link comes in. However, despite the popular neuro-myth, turkey is actually no higher in tryptophan concentration than other types of poultry. Numerous different plant and animal proteins provide us with our daily doses of tryptophan, with sunflower seeds, egg whites and soy beans having some of the highest concentrations of the amino acid. In fact, turkey comes in at a measly 10th on the list of tryptophan sources.

Instead, the relation between eating and sleeping seems to be more dependent on the amount of food consumed, rather than the type we eat. Insulin is released after every meal, particularly ones high in carbohydrates, and the more carbs consumed, the more insulin is produced. This increase then changes the chemical levels in our bloodstream, affecting the re-uptake and release of various amino acids. Ultimately these changes result in greater amounts of tryptophan crossing the blood-brain-barrier and being taken up into the brain. There the tryptophan is converted to serotonin, some of which is also metabolized into melatonin, causing our postprandial nap.

Tryptophan’s influence on serotonin levels doesn’t just affect sleep cycles. The link between depression and low serotonin levels is well established, and tryptophan supplements have been suggested as less invasive treatments for the disorder. Unfortunately these studies have been mostly unsuccessful to date, as mild modifications of tryptophan seem to have little to no effect on mood in most individuals. However, it is possible that people with low endogenous levels of tryptophan due to specific genetic profiles may be more susceptible to the chemical’s effect on mood, and current research is still ongoing in the matter.

So regardless of whether it’s turkey, stuffing or sweet potatoes you prefer, remember to load up your plate during Thanksgiving to get those happy drowsy effects later. It may just help you feel a little bit calmer, and prevent some of the Black Friday mayhem the next day.

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In honor of the 4th of July and in the spirit of the Declaration of Independence, The Atlantic published a nice piece on the “Pursuit of Happiness” this week, specifically on how our community and environment can shape our mood and mindset, and how local governments are initiating public service projects to aid in our psychological well-being. However, a study published in the Journal of Human Geneticslast month by behavioral economists at the London School of Economics suggests that it is not external factors but rather our genes and neurotransmitters (most notably serotonin) that determine how happy we are.

Serotonin has been linked to happiness and empathy, and a depletion of it is often seen in patients with depression. Many common antidepressants work by elevating levels of serotonin in the brain, including SSRIs (selective serotonin reuptake inhibitors), the most commonly prescribed medication for depression, which prevents the retraction of serotonin back into the cell after it has been released. This recycling of serotonin occurs naturally in the brain, with neurotransmitter transporters binding to the chemical in the synapse, taking the serotonin back up into the cell, and enabling it to be released again. The serotonin transporter gene 5-HTT is involved in the expression of the proteins that form these transporters and has two different forms it can take, a long or a short version. The long allele of 5-HTT results in more transporters being expressed, however, paradoxically, researchers have recently discovered that individuals who carry two long versions of the gene are significantly more likely to report higher levels of subjective well-being than those who inherited two short versions of the allele. In the study by Dr. Jan-Emmanuel De Neve, 69% of those with the long versions rated themselves as either satisfied or very satisfied with their lives, as opposed to only 38% of people with the short versions. While this is contradictory to the theory behind SSRIs, which prevent the recycling of the neurochemical and thus enable higher levels of serotonin to be present in the synapses, the greater number of transporters in the long allele population permits faster turn-over, facilitating greater release and higher, more stable levels in the brain.

On the other end of the spectrum, individuals with short alleles are known to have decreased brain density in the amygdala and limbic circuitry, areas implicated in emotion regulation and fear responses, impairing their perception and reaction to emotional stimuli. Those with short alleles have a higher risk of depression, although this association is somewhat tenuous as the 5-HTT gene directly only accounts for 10% of an individual’s susceptibility to anxiety or depression. Most likely, it is a gene-environment interaction that determines an individual’s likelihood of developing depression, as individuals with short alleles are more prone to react poorly or with greater anxiety to bad news.

Thus, returning to The Atlantic article, to what extent can our environment really foster a positive affect, and do things like city planning–improving traffic flow or building green spaces–really influence our overall levels of happiness? How much do the little things in our environment matter? Sure it’s unpleasant to sit in traffic and much more agreeable to eat lunch under a tree, but in the greater manifestation of mood do these things affect us on such a fundamental level? After the immediate physical or aesthetic enjoyment, are there pervasive lingering effects? Surely it is more the people we surround ourselves with and our own internal perception of events that determines our mood. How much of an effect do we have on our own happiness and how much is determined by our surroundings? What truly makes us happy?